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Notes: We have prepared the superconducting compound YBa2Cu3O7−x through a melt process. Solidification of this material at cooling rates 〈105 K/s yields BaCuO2 and a previously unreported metastable phase which indexes to a cubic pattern with a lattice constant of 0.701 nm. Faster solidification rates yield only the cubic phase and glassy materials. Annealing these materials in O2 gives rise to a single-phase material of the YBa2Cu3O7−x orthorhombic structure. The material has zero resistance at 91.6 K with a transition width of 1.4 K. The grain size of the materials after annealing averages 10 μm in length and 2–3 μm in width, and the grains are compositionally homogeneous. Twins are seen with spacings on the order of 20 nm. The irreversibility of the magnetization curve at low temperatures can be ascribed to strong flux pinning mechanisms.

Notes: The superconducting YBa2Cu3O7−x phase has been produced through a novel rapid solidification processing route yielding a high-quality granular superconducting phase. Features in the magnetic susceptibility as measured at various fields can be attributed to important transitions in the superconducting behavior of these materials. At low fields (∼20 Oe) anomalies in the susceptibility arise from decoupling of the grains in these polycrystalline materials. Susceptibility response at higher fields (∼100 Oe) is representative of randomly oriented superconducting grains which show local superconducting current densities comparable to those of single crystals. At even higher fields features consistent with Muller's superconducting glass state model are observed.

Notes: Background: The nephron reduction in IgA nephropathy is critical for the newly established prognosis of this disease. A high immunoglobulin A inbred strain of ddY mouse (HIGA mouse) showed progressive mesangial sclerosis with elevated renal expression of transforming growth factor (TGF)-β,1 however, the progression of the renal lesion of this mouse is relatively mild with rare association of active crescentic glomerulonephritis. However, although nephron reduction causes progressive renal injury, the modifications of glomerular lesions by nephron reduction are dependent upon the pathological background of each strain. Thus, we investigated the influence of nephron reduction by heminephrectomy on the renal lesions of the HIGA mouse.Methods: Five-week-old HIGA mice were heminephrectomized (Nx), and were evaluated in comparison with a sham-operated group (S) at 40 weeks old. Measurements of renal function, blood pressure and serum levels of immunoglobulins (IgG, IgA, and IgM) were performed. Histological findings, including glomerular enlargement, matrix expansion, immunoglobulin depositions (IgG, IgA, and IgM), expressions of cytokines (TGF-β, TNF-α, and IL-6) and extracellular matrix proteins were analysed. PCNA and TUNEL stainings were performed. In addition, mRNA expressions of renin-angiotensin systems (RAS; angiotensinogen and angiotensin converting enzyme (ACE)) were also investigated.Results: The physiological and serological data showed no significant difference between Nx and S. In Nx, the glomerular tuft area and ratio of mesangial matrix area for one tuft were significantly increased and glomerular IgG and IgM deposits were significantly expanded in the paramesangium. However, IgA was not significantly increased. The glomerular expressions of cytokines (TGF-β, TNF-α, and IL-6) and extracellular matrix proteins (fibronectin, collagen type I and IV) were significantly increased in this group. In contrast to the significant decrease of PCNA-positive cells, TUNEL-positive cells were significantly increased in Nx. The total mRNA expression of ACE was also significantly increased in the renal cortex of Nx.Conclusion: Heminephrectomy of HIGA mice may be a potential model for the research into the progressive glomerulosclerosis of human IgA nephropathy. The pathological role of apoptosis is apparently involved in these disease processes, possibly through up-regulated RAS.

Notes: Fibrin deposition is often noted in mesangial areas in active types of human mesangioproliferative glomerulonephritis; IgA nephropathy or Henoch-Schönlein purpura nephritis.1,2In vivo, mesangial cells are provided with various coagulation factors from blood circulation through fenestration of glomerular capillary endothelium. Factor V in its active form (Va) officiates as a membrane-bound cofactor to factor Xa, forming prothrombinase complex Xa/Va, which converts prothrombin to thrombin. In the present study, to clarify the contribution of factor V in intramesangial coagulation, mesangial factor V expression and its relationship to mesangial proliferation was investigated.Cross-linked fibrin (XFb) was detected in renal biopsy specimens from the patients of IgA nephropathy using anti-d-dimer antibody combined with plasmin exposure,1 and factor V was detected with rabbit antibody against human factor V. The expression of factor V mRNA was assessed by in situ hybridization in relation to the simultaneous antigen staining of alpha-smooth muscle actin (α-SMA). For in vitro study, cultured human mesangial cells (MCs) were stimulated with TNF-α (100 U/mL), and immunocytochemically stained the factor V protein, or evaluated by Western blot analysis. In another experiment, starved MCs were further incubated in combination with factor Xa, prothrombin, fibrinogen and factor XIII, and fibrin production on MCs was assessed. In a blocking test using an antibody against factor V, suppression of fibrin production was evaluated.XFb deposition and factor V expression were markedly correlated with disease activity (〈link href="#t1"〉Table 1). By in situ hybridization, factor V mRNA was detected mainly in the mesangial cells which were positive for α-SMA, and partly in endothelial cells. In vitro study revealed that factor V expression was elevated time-dependently after TNF-α stimulation (P 〈 0.01), and that fibrin production on TNF-α-stimulated MCs was increased (P 〈 0.0001), and inhibited by the addition of antifactor V antibody (P 〈 0.01).〈tabular xml:id="t1"〉1〈title type="main"〉 Relationship of XFb deposition and factor V expression to histological and immunohistochemical findings 〈table frame="topbot"〉〈tgroup cols="3" align="left"〉〈colspec colnum="1" colname="col1" align="left"/〉〈colspec colnum="2" colname="col2" align="char" char="."/〉〈colspec colnum="3" colname="col3" align="char" char="."/〉〈thead valign="bottom"〉〈entry align="center"〉 P value vs XFb〈entry align="center"〉 P value vs〈row rowsep="1"〉〈entry align="center"/〉〈entry align="center"〉factor V〈tbody valign="top"〉Mesangial cell proliferation0.020.04Necrotizing lesion0.020.03Cellular crescent0.020.03Interstitial mononuclear
 infiltrate0.040.07Activity index0.0050.008In conclusion, factor V is expressed in mesangial cells after stimulation by inflammation, and may exert procoagulant activity in cooperation with exogenous factor Xa, leading to intramesangial coagulation in IgA nephropathy.